Electric stimulation of the vagus nerve reduced mouse neuroinflammation induced by lipopolysaccharideReport as inadecuate




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Journal of Inflammation

, 13:33

First Online: 29 October 2016Received: 30 August 2016Accepted: 11 October 2016

Abstract

BackgroundNeuroinflammation NI is a key feature in the pathogenesis and progression of infectious and non-infectious neuropathologies, and its amelioration usually improves the patient outcome. Peripheral inflammation may promote NI through microglia and astrocytes activation, an increased expression of inflammatory mediators and vascular permeability that may lead to neurodegeneration. Several anti-inflammatory strategies have been proposed to control peripheral inflammation. Among them, electrical stimulation of the vagus nerve VNS recently emerged as an alternative to effectively attenuate peripheral inflammation in a variety of pathological conditions with few side effects.

Considering that NI underlies several neurologic pathologies we explored herein the possibility that electrically VNS can also exert anti-inflammatory effects in the brain.

MethodsNI was experimentally induced by intraperitoneal injection of bacterial lipopolysaccharide LPS in C57BL-6 male mice; VNS with constant voltage 5 Hz, 0.75 mA, 2 ms was applied for 30 s, 48 or 72 h after lipopolysaccharide injection. Twenty four hours later, pro-inflammatory cytokines IL-1β, IL-6, TNFα levels were measured by ELISA in brain and spleen extracts and total brain cells were isolated and microglia and macrophage proliferation and activation was assessed by flow cytometry. The level of ionized calcium binding adaptor molecule Iba-1 and glial fibrillary acidic protein GFAP were estimated in whole brain extracts and in histologic slides by Western blot and immunohistochemistry, respectively.

ResultsVNS significantly reduced the central levels of pro-inflammatory cytokines and the percentage of microglia CD11b-CD45 and macrophages CD11b-CD45, 24 h after the electrical stimulus in LPS stimulated mice. A significantly reduced level of Iba-1 expression was also observed in whole brain extracts and in the hippocampus, suggesting a reduction in activated microglia.

ConclusionsVNS is a feasible therapeutic tool to attenuate the NI reaction. Considering that NI accompanies different neuropathologies VNS is a relevant alternative to modulate NI, of particular interest for chronic neurological diseases.

KeywordsNeuroinflammation Microglia Lipopolysaccharide neuropathologies Stimulation of vagus nerve Antiinflammatory AbbreviationsAchAcetylcholine

BBBBlood-brain barrier

BSAIsotonic bovine seroalbumin

CNSCentral nervous system

GFAPGlial fibrillary acidic protein

GKNGlucose–potassium–sodium

Iba-1Ionized calcium binding adaptor molecule 1

ipIntraperitoneally

LPSLipopolysaccharide

NINeuroinflammation

TMB3,3’5,5’ Tetrametil-bencidina

VNSElectrical stimulation of the vagus nerve

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Author: G. Meneses - M. Bautista - A. Florentino - G. Díaz - G. Acero - H. Besedovsky - D. Meneses - A. Fleury - A. Del Rey - G.

Source: https://link.springer.com/







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